Pacemaker Syndrome Differential Diagnoses

  • Author: Daniel M Beyerbach, MD, PhD; Chief Editor: Jeffrey N Rottman, MD   more...
 
Updated: Jan 4, 2012
 
 

Differential Diagnoses

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Contributor Information and Disclosures
Author

Daniel M Beyerbach, MD, PhD  Medical Director, Cardiac Rhythm Program, The Christ Hospital; Affiliate Clinical Assistant Professor of Biomedical Science, Florida Atlantic University

Daniel M Beyerbach, MD, PhD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Coauthor(s)

Christopher Cadman, MD  Director of Arrhythmia Service, Assistant Professor, Department of Internal Medicine, Division of Cardiology, University of New Mexico

Christopher Cadman, MD is a member of the following medical societies: American College of Cardiology and Phi Beta Kappa

Disclosure: Nothing to disclose.

Specialty Editor Board

Hanumant Deshmukh, MD †  Former Chief of Cardiology, Veterans Affairs Medical Center; Former Associate Professor, Department of Medicine, Rosalind Franklin University of Medicine and Science

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Brian Olshansky, MD  Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

Amer Suleman, MD  Private Practice

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD  Professor of Medicine and Pharmacology, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)

Disclosure: Nothing to disclose.

References

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Pronounced PR interval prolongation. The effect of this PR interval prolongation on AV dyssynchrony is demonstrated in this ECG image.
AV dyssynchrony resulting from severe PR interval prolongation in the setting of sinus rhythm. In this ECG, the PR interval is prolonged to the point that the P wave occurs coincident with the peak of the T wave. Compare to the prior image of the same patient with a slower sinus rate.
Accelerated idioventricular rhythm with retrogradely conducted P waves. This ECG demonstrates a mechanism of AV dyssynchrony that might lead to pseudopacemaker syndrome.
Junctional rhythm with retrogradely conducted P waves. If symptoms of pacemaker syndrome develop, increasing the lower rate limit for pacing may help to restore AV synchrony.
Retrogradely conducted P waves are visible directly following each ventricular-paced complex.
This is an ECG tracing of a patient with continuous atrioventricular synchronous (DDD) pacing prior to development of symptoms. Atrial stimulation (open arrows) is followed by visible P waves. Wide QRS complexes follow ventricular stimulation (solid arrows).
This is an ECG tracing of a patient with atrioventricular (AV) dissociation and resultant pacemaker syndrome. Native atrial depolarizations (arrows) move progressively closer to pacemaker-stimulated ventricular depolarizations. Ventricular pacemaker stimuli (arrowheads) are greater in amplitude than those visible in the previous image, consistent with mode reversion from AV synchronous (DDD) to ventricular inhibited (VVI), which includes a switch from bipolar pacing (low amplitude) to unipolar pacing (higher amplitude).
Table. Incidence of Atrial Fibrillation in Patients with Pacemakers
Study Patients



(number)



Total Incidence



(%)



Follow-up



(years)



Annual Incidence



(%)



VVI AAI DDD VVI AAI DDD
Frielingsdorf[25] 1838 18-47 0-17* 3.75 4.8-12.5 0-4.5*
Sutton and Kenny[26] 1061 22 3.9 AAI: 2.75



VVI: 3.25



6.77 1.42
Hesselson[27] 8827 14-57 0-23 AAI: 1-8



VVI: 3-8



Cannot be determined
Hesselson[27] 950 38 7 7 5.43 1.00
Santini[28] 339 48 3.7 13 5 9.6 0.74 2.6
Sasaki[29] 75 41 2* AAI: 3.25



VVI: 5.17



7.9 0.62*
Rosenqvist[30] 168 47 6.7 4 11.8 1.68
*Combined AAI and DDD
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